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    Proceedings of the National Academy of Sciences ; 1996
    In:  Proceedings of the National Academy of Sciences Vol. 93, No. 26 ( 1996-12-24), p. 15341-15345
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 93, No. 26 ( 1996-12-24), p. 15341-15345
    Kurzfassung: It has been demonstrated that CD8 + T cells produce a soluble factor(s) that suppresses human immunodeficiency virus (HIV) replication in CD4 + T cells. The role of soluble factors in the suppression of HIV replication in monocyte/macrophages (M/M) has not been fully delineated. To investigate whether a CD8 + T-cell-derived soluble factor(s) can also suppress HIV infection in the M/M system, primary macrophages were infected with the macrophage tropic HIV-1 strain Ba-L. CD8 + T-cell-depleted peripheral blood mononuclear cells were also infected with HIV-1 IIIB or Ba-L. HIV expression from the chronically infected macrophage cell line U1 was also determined in the presence of CD8 + T-cell supernatants or β-chemokines. We demonstrate that: ( i ) CD8 + T-cell supernatants did, but β-chemokines did not, suppress HIV replication in the M/M system; ( ii ) antibodies to regulated on activation normal T-cell expressed and Secreted (RANTES), macrophage inflammatory protein 1α (MIP-1α) and MIP-1β did not, whereas antibodies to interleukin 10, interleukin 13, interferon α, or interferon γ modestly reduced anti-HIV activity of the CD8 + T-cell supernatants; and ( iii ) the CD8 + T-cell supernatants did, but β-chemokines did not, suppress HIV-1 IIIB replication in peripheral blood mononuclear cells as well as HIV expression in U1 cells. These results suggest that HIV-suppressor activity of CD8 + T cells is a multifactorial phenomenon, and that RANTES, MIP-1α, and MIP-1β do not account for the entire scope of CD8 + T-cell-derived HIV-suppressor factors.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1996
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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